The interaction between the inflammatory and immune systems has traditionally focused on the action of activated complement proteins and lymphokines on the cells mediating inflammation; by contrast, we will examine the influence of the acute inflammatory reactant, C-reactive protein (CRP), on the immune functions of lymphoid cells. Although elevated levels of CRP are an accompaniment of a wide variety of diseases, its biological role in host defense is still unknown. To delineate the effects of CRP on immune functions we will use the T-cell specific binding property of CRP to isolate CRP-binding cells and characterize their surface antigens and receptors. Analysis of the influence of CRP on anti-tumor immune reactivities stems from our observations of the activation of nonspecific suppressor mouse T-cells and will include tests of the ability of CRP to not only limit sensitization to tumor antigens, but also the expression of tumor specific immune reactivity in vitro and in vivo. Tumor specific cell-mediated immune reactivity of breast cancer patients and mice will be studied to determine the cellular mechanism of suppression by CRP. Binding of CRP to lymphoid cells that have infiltrated regressing and progressing animal tumors will be measured. CRP will be compared to interferon and interferon inducers both as an activator of macrophages to the tumoricidal level and as an augmentor of NK cell activity. The perspective for comparison with interferon is the analogous induction of both substances. Eventually we hope to elucidate ways by which CRP can be manipulated clinically to the advantage of the host and its serum levels interpreted in a meaningful way.